Tremella fuciformis polysaccharide suppresses hydrogen peroxide-triggered injury of human skin fibroblasts via upregulation of SIRT1.

Tremella fuciformis polysaccharide suppresses hydrogen peroxide-triggered injury of human skin fibroblasts via upregulation of SIRT1.
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银耳多糖通过上调 SIRT1 抑制过氧化氢引发的人皮肤成纤维细胞损伤

DOI:
10.3892/mmr.2017.6754
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发表时间:
2017-08
影响因子:
3.4
通讯作者:
Wang C
Wang C
中科院分区:
医学4区
文献类型:
--
作者:
Shen T;Duan C;Chen B;Li M;Ruan Y;Xu D;Shi D;Yu D;Li J;Wang C

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银耳多糖(Tremella fuciformis polysaccharide,TFPS)是银耳的提取物,具有抗氧化、抗炎、抗衰老等作用。然而,这些保护和治疗作用的机制仍有待阐明。本研究的目的是探讨TFPS对过氧化氢诱导的人皮肤成纤维细胞损伤的保护作用,并阐明上述潜在的机制。首次建立了过氧化氢诱导的人皮肤成纤维细胞损伤模型。MTT和活性氧(ROS)的产生测定,除了末端脱氧核苷酸转移酶dUTP缺口末端标记,逆转录-定量聚合酶链反应和蛋白质印迹,进行研究TFPS的保护作用。过氧化氢降低人皮肤成纤维细胞活力,同时增加ROS生成和细胞凋亡。单独用0-400 μg/ml TFPS处理长达48小时不会导致细胞活力改变。值得注意的是,TFPS预处理减少过氧化氢处理的皮肤成纤维细胞中的氧化应激和细胞凋亡。此外,有深刻的抑制p16,p21,p53和caspase-3的表达,并激活细胞外信号调节激酶和Akt丝氨酸/苏氨酸激酶1,TFPS预处理后。此外,还发现TFPS还通过SIRT 1表达的上调来保护成纤维细胞,并且这被SIRT 1抑制剂烟酰胺废除。这些结果表明,TFPS减轻过氧化氢诱导的氧化应激和细胞凋亡的皮肤成纤维细胞通过上调SIRT 1的表达,表明TFPS可能作为一个潜在的治疗剂氧化应激相关的皮肤疾病和老化。
Tremella fuciformis polysaccharide (TFPS), which is the extract of Tremella fuciformis Berk, has previously been demonstrated to exhibit potent anti-oxidative, anti-inflammatory and anti-aging effects. However, the mechanisms underlying these protective and therapeutic effects remain to be elucidated. The aim of the present study was to investigate the protective effects of TFPS on hydrogen peroxide-induced injury of human skin fibroblasts and to elucidate the aforementioned underlying mechanisms. A hydrogen peroxide-induced human skin fibroblast injury model was firstly established. MTT and reactive oxygen species (ROS) production assays, in addition to terminal deoxynucleotidyl transferase dUTP nick end labeling, reverse transcription-quantitative polymerase chain reaction and western blotting, were performed to investigate the protective effects of TFPS. Hydrogen peroxide decreased human skin fibroblast viability with a concurrent increase in ROS generation and cell apoptosis. Treatment with 0–400 µg/ml TFPS alone for up to 48 h did not result in alteration in cell viability. Notably, TFPS pre-treatment reduced oxidative stress and cell apoptosis in hydrogen peroxide-treated skin fibroblasts. In addition, there was profound inhibition of p16, p21, p53 and caspase-3 expression, and activation of extracellular-signal regulated kinase and Akt serine/threonine kinase 1, following TFPS pre-treatment. Furthermore, it was revealed that TFPS additionally protected fibroblasts via the upregulation of SIRT1 expression, and this was abrogated by the SIRT1 inhibitor niacinamide. These results indicated that TFPS alleviated hydrogen peroxide-induced oxidative stress and apoptosis in skin fibroblasts via upregulation of SIRT1 expression, indicating that TFPS may act as a potential therapeutic agent for oxidative-stress-associated skin diseases and aging.
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